Nitric Oxide and Synaptic Function

Schuman, Erin M.; Madison, Daniel V.

doi:10.1146/annurev.ne.17.030194.001101

Cited by 753 publications

(292 citation statements)

References 151 publications

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“…Nitric oxide (NO) is an important messenger molecule implicated in multiple physiological and pathophysiological events in the central nervous system (Moncada et al, 1991;Schuman & Madison, 1994). NO is synthesized from Larginine by NO synthase in response to Ca 2+ entry through the activated N-methyl-D-aspartate (NMDA) receptor-gated ion channels.…”

Section: Introductionmentioning

confidence: 99%

“…NO di uses rapidly and, as shown particularly in the cerebellum of rodents, exerts its action in surrounding target cells by increasing cyclic GMP levels (Garthwaite et al, 1988, Schuman & Madison, 1994. It seems likely that NO acts via cyclic GMP dependent mechanisms by modulating the release of various neurotransmitters (Prast et al, 1994;Schuman & Madison, 1994), e.g., NO has been shown to enhance the striatal dopamine release (Bowyer et al, 1995;Stewart et al, 1996). NMDA receptor-mediated neurotransmitter release is regulated, in part, through NO production and can be blocked by NO synthase inhibitors (Dawson & Dawson 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Four distinct isoforms of NO synthase have been identi®ed (Schuman & Madison, 1994). N G -nitro-L-arginine (L-NNA) and N G -nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole inhibit endothelial and neuronal NO synthase isoforms (Moore et al, 1991;Moore & Handy, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…N G -nitro-L-arginine (L-NNA) and N G -nitro-L-arginine methyl ester (L-NAME) and 7-nitroindazole inhibit endothelial and neuronal NO synthase isoforms (Moore et al, 1991;Moore & Handy, 1997). Depending on the used compound, dose and pretreatment time, there are con¯icting data on e ects of NO synthase inhibitors in animal models of epilepsy, parkinsonism or cerebral ischaemia (Eblen et al, 1996;Rundfeldt et al, 1995;Schuman & Madison, 1994). Therefore, in the present study, we examined the e ects of di erent NO synthase inhibitors, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Antidystonic efficacy of nitric oxide synthase inhibitors in a rodent model of primary paroxysmal dystonia

Richter

Löschmann²,

Löscher

2000

British J Pharmacology

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1 In a hamster model (genetic symbol dt sz ) of primary paroxysmal non-kinesiogenic dystonic choreoathetosis, recent studies have shown bene®cial e ects of glutamate and dopamine receptor antagonists. Nitric oxide (NO), synthesized from L-arginine by NO synthase in response to glutamate receptor activation, elicits cyclic GMP and modulates glutamate-mediated processes and striatal dopamine release. 2 Therefore, the e ects of NO synthase inhibitors and of L-arginine on severity of dystonia were investigated in dt sz hamsters in which dystonic attacks, characterized by twisting movements and postures, can be induced by stress.arginine methyl ester (L-NAME) and 7-nitroindazole signi®cantly reduced the severity of dystonia. At antidystonic e ective doses neither L-NNA nor L-NAME caused observable side e ects, whereas 7-nitroindazole exerted moderate reduction of locomotor activity. 4The antidystonic e ect of L-NAME was reversed by co-administration of the NO precursor Larginine. However, L-arginine administered alone did not exert any e ect on severity of dystonia. 5 Cerebellar cyclic GMP levels in brains of mutant hamsters in comparison to non-dystonic control hamsters did not signi®cantly di er, but the cerebellar cyclic GMP levels tended to be increased in dt sz hamsters during a dystonic attack. L-NAME signi®cantly decreased the cerebellar cyclic GMP levels in both dt sz and control hamsters. 6 Although an overproduction of NO is probably not critically involved in the pathogenesis of paroxysmal dystonia, it may contribute to the manifestation of dystonic attacks, as indicated by the antidystonic e ects of NO synthase inhibitors. 7 Peripheral side e ects may limit the clinical use of NO synthase inhibitors, but more selective inhibitors of the neuronal NO synthase should be considered as interesting candidates for the treatment of paroxysmal dystonia. British Journal of Pharmacology (2000) 131, 921 ± 926

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Antidystonic efficacy of nitric oxide synthase inhibitors in a rodent model of primary paroxysmal dystonia

Richter

Löschmann²,

Löscher

2000

British J Pharmacology

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“…It acts as an unconventional neuronal messenger and is synthesized on demand (for review, see Steinbusch et al, 2000). It is generated by NO synthase (NOS), an enzyme expressed by discrete neuronal populations throughout the nervous system (Schuman and Madison, 1994). Aberrant synthesis and interactions of NO with other molecules are thought to underlie a number of neurodegenerative processes and CNS disorders (for reviews, see Schulz et al, 1995;Wolf, 1997).…”

mentioning

confidence: 99%

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

et al. 2002

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When vestibular damage occurs, nitric oxide synthase (NOS) expression in rat cerebellar flocculus is affected. Since compensation for postural symptoms occurs and Purkinje cells play an important role in movement coordination and motor learning, we analyzed in situ the induction of NOS in the Purkinje cell population of the cerebellum (corpus cerebelli) of frog after unilateral transection of the eighth statoacoustic nerve to gain insight into the role of NO in neural plasticity after injury. Three days after neurectomy, the early effects induced NADPH diaphorase reactivity in most of the Purkinje cells on the ipsilateral side, while on the contralateral side the highest labeling was observed at 15 days. This finding can give information on the dynamics of vestibular compensation, in which NOS involvement was investigated. At 30 days, NADPH diaphorase reactivity was present in a large number of Purkinje cells of the whole cerebellum, while at 60 days a down-regulation for NADPH diaphorase reactivity was evident. A similar trend was observed for NOS-immunoreactivity, which was still present at 60 days in a high percentage of Purkinje cells, mainly on the ipsilateral side. On the basis of cell density evaluations, it was proposed that the early induction of NOS after neurectomy was linked to the degeneration of a part of the Purkinje neurons, while the permanence of NOS labeling might be due to a neuroprotective role of NO in the restoration phase of the vestibular compensation process. Anat Rec 268: 73-83, 2002.

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NADPH-Diaphorase activity changes during gangliogenesis and metamorphosis in the gastropod molluscIlyanassa obsoleta

Lin

Leise

1996

J. Comp. Neurol.

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Gaseous nitric oxide (NO) is produced through the action of the enzyme nitric oxide synthase (NOS) and acts as a neurotransmitter (Jacklet and Gruhn, 1994b;Elphick et al., 1995a;Jacklet, 1995) in the nervous systems of adult gastropod molluscs. By comparison, little or no information appears to exist about the ontogeny of molluscan NOS-containing neurons. NADPH-diaphorase (NADPHd) has been determined biochemically and histochemically to colocalize with NOS immunoreactivity in neurons; NOS is an isoform of NADPHd (Dawson et al., 1991;Hope et al., 1991). We used NADPHd histochemistry to map the distribution of NOS activity in the nervous systems of larvae, including metamorphosing individuals, and juveniles of the marine snail Ilyanassa obsoleta. Several ganglionic neuropils displayed reaction product throughout development. The most intense NADPHd staining occurred in the neuropil of the apical ganglion, a specialized larval structure. Intermediate staining levels occurred in neuropils of the cerebral, pedal, and pleural ganglia. Larval buccal and intestinal ganglia showed little reaction product, with slight increases arising in metamorphically competent larvae. NADPHd activity conspicuously decreased in the central nervous systems of metamorphosing larvae. The osphradial ganglion, which was present in young larvae, showed only weak NADPHd activity. Our results provide evidence for the existence of a nitrergic signalling system in molluscan larvae and juveniles.

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Nitric Oxide and Synaptic Function

Cited by 753 publications

References 151 publications

Antidystonic efficacy of nitric oxide synthase inhibitors in a rodent model of primary paroxysmal dystonia

Antidystonic efficacy of nitric oxide synthase inhibitors in a rodent model of primary paroxysmal dystonia

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

NADPH-Diaphorase activity changes during gangliogenesis and metamorphosis in the gastropod molluscIlyanassa obsoleta

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